Neutrophil (PMN) sequestration in the pulmonary microvasculature precedes the migration of these cells into the airspaces in inflamed lungs. Intratracheal instillation of the heat-killed organism Corynebacterium parvum in the rat induces an alveolitis in which PMN constitute 70 to 80% of the total cell count in the bronchoalveolar lavage (BAL). This acute alveolitis results in increased sequestration in the pulmonary microvasculature of 51Cr-labeled PMN when compared with control lungs. The aims of this study were to confirm this increased pulmonary PMN sequestration using unlabeled cells and to assess the function and adhesion molecule expression of such sequestered PMN. We counted the number of PMN and erythrocytes obtained by pulmonary vascular lavage (PVL) and compared the ratio of these two cell types in PVL and peripheral blood (PB) as a measure of the sequestration of PMN in the pulmonary vasculature. Compared with control animals, PVL in C. parvum-treated rats had higher PMN counts, which could not be accounted for by the PB leukocytosis. Sequestration of PMN in the pulmonary microvasculature depends on several factors, including the upregulation of adhesion molecules on both PMN and endothelial surfaces and the ability of the cells to deform when passing through the microcirculation. Cells obtained from the PVL were less deformable than PB cells in control but not in C. parvum-treated animals. The expression of the CD18 integrin on PMN obtained from the PVL of C. parvum-treated animals was increased compared with cells from control animals.(ABSTRACT TRUNCATED AT 250 WORDS)